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10.1038/s41598-017-03237-3 http://scihub22266oqcxt.onion/10.1038/s41598-017-03237-3 C5469816!5469816!28611444     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28611444|t=2017. EP4 inhibition attenuates the development of diabetic and non-diabetic experimental kidney disease |pdf=|usr=}}{{28611444}} gab.com Text EP4 inhibition attenuates the development of diabetic and non-diabetic experimental kidney disease JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28611444 #FOAvip The therapeutic targeting of prostanoid subtype receptors may slow the development of chronic kidney disease (CKD) through mechanisms that are distinct from those of upstream COX inhibition. Here, employing multiple experimental models of CKD, we studied the effects of inhibition of the EP4 receptor, one of four receptor subtypes for the prostanoid prostaglandin E2. In streptozotocin-diabetic endothelial nitric oxide synthase knockout mice, EP4 inhibition attenuated the development of albuminuria, whereas the COX inhibitor indomethacin did not. In Type 2 diabetic db/db mice, EP4 inhibition lowered albuminuria to a level comparable with that of the ACE inhibitor captopril. However, unlike captopril, EP4 inhibition had no effect on blood pressure or hyperfiltration although it did attenuate mesangial matrix accumulation. Indicating a glucose-independent mechanism of action, EP4 inhibition also attenuated proteinuria development and glomerular scarring in non-diabetic rats subjected to surgical renal mass ablation. Finally, in vitro, EP4 inhibition prevented transforming growth factor-ß1 induced dedifferentiation of glomerular podocytes. In rodent models of diabetic and non-diabetic CKD, EP4 inhibition attenuated renal injury through mechanisms that were distinct from either broadspectrum COX inhibition or ?standard of care? renin angiotensin system blockade. EP4 inhibition may represent a viable repurposing opportunity for the treatment of CKD. Twit Text FOAVip EP4 inhibition attenuates the development of diabetic and non-diabetic experimental kidney disease ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28611444 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28611444 #FOAvip English Wikipedia <ref>{{Cite pmid|28611444}}</ref> EP4 inhibition attenuates the development of diabetic and non-diabetic experimental kidney disease #MMPMID28611444 Thieme K; Majumder S; Brijmohan AS; Batchu SN; Bowskill BB; Alghamdi TA; Advani SL; Kabir MG; Liu Y; Advani A Sci Rep 2017[]; 7 (ä): ä PMID28611444show ga The therapeutic targeting of prostanoid subtype receptors may slow the development of chronic kidney disease (CKD) through mechanisms that are distinct from those of upstream COX inhibition. Here, employing multiple experimental models of CKD, we studied the effects of inhibition of the EP4 receptor, one of four receptor subtypes for the prostanoid prostaglandin E2. In streptozotocin-diabetic endothelial nitric oxide synthase knockout mice, EP4 inhibition attenuated the development of albuminuria, whereas the COX inhibitor indomethacin did not. In Type 2 diabetic db/db mice, EP4 inhibition lowered albuminuria to a level comparable with that of the ACE inhibitor captopril. However, unlike captopril, EP4 inhibition had no effect on blood pressure or hyperfiltration although it did attenuate mesangial matrix accumulation. Indicating a glucose-independent mechanism of action, EP4 inhibition also attenuated proteinuria development and glomerular scarring in non-diabetic rats subjected to surgical renal mass ablation. Finally, in vitro, EP4 inhibition prevented transforming growth factor-ß1 induced dedifferentiation of glomerular podocytes. In rodent models of diabetic and non-diabetic CKD, EP4 inhibition attenuated renal injury through mechanisms that were distinct from either broadspectrum COX inhibition or ?standard of care? renin angiotensin system blockade. EP4 inhibition may represent a viable repurposing opportunity for the treatment of CKD. äEP4 inhibition attenuates the development of diabetic and non-diabetic(epmc).pdf DeepDyve Pubget Overpricing